CMC8 - Current Medicinal Chemistry 2001, 8, 829-838 829...

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Current Medicinal Chemistry 2001 , 8, 829-838 829 Oxidative Stress and Antioxidants in Exercise C. Leeuwenburgh* 1 and J. W. Heinecke 2 1 Center for Exercise Science, Aging Biochemistry Laboratory, College of Health and Human Performance, University of Florida, Gainesville, FL 32611, USA 2 Department of Internal Medicine and Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA Abstract : Increased aerobic metabolism during exercise is a potential source of oxidative stress. In muscle, mitochondria are one important source of reactive intermediates that include superoxide (O 2 - ), hydrogen peroxide (H 2 O 2 ), and possibly hydroxyl radical (HO ). The recent discovery that mitochondria may generate nitric oxide (NO ) also has implications for oxidant production and mitochondrial function. In this review, we critically examine the concept that production of reactive intermediates increases during exercise. Because the health benefits of regular exercise are well-documented, we also examine adaptations to exercise that may decrease oxidative stress. These include increased antioxidant defenses, reduced basal production of oxidants, and reduction of radical leak during oxidative phosphorylation. INTRODUCTION membrane-associated NADPH oxidase to generate O 2 - , which can directly react with target compounds or dismutate to H 2 O 2 . Peroxide in turn is converted to hypochlorous acid (HOCl) by myeloperoxidase, a heme protein secreted by neutrophils and monocytes [15,16]. HOCl is an inflammatory mediator and a strongly oxidizing and chlorinating compound that generates other reactive metabolites such as nitryl chloride (NO 2 Cl) in the presence of nitrite [17]. Moreover, activated human polymorphonuclear neutrophils can use myeloperoxidase and H 2 O 2 to convert nitrite into nitrogen dioxide radical (NO 2 ), contributing to the formation of potentially harmful compounds [17]. The well-documented benefits of regular physical exercise include reduced risk of cardiovascular disease, cancer, osteoporosis, and diabetes [1-3]. The complex mechanisms that contribute to these effects include decreased adipose tissue, altered lipid and hormonal profiles, receptor and transport-protein adaptations, improved mitochondrial coupling, and alterations to antioxidant defenses. Such defenses are necessary because aerobic organisms produce reactive oxygen species during normal respiration and inflammatory conditions. Exercise can create an imbalance between oxidant and antioxidant levels, a situation known as oxidative stress. Indeed, oxidative stress resulting from acute exercise in unadapted and adapted subjects has been proposed to damage enzymes, protein receptors, lipid membranes, and DNA [4-8]. Although endothelial cells, leukocytes, alterations in
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CMC8 - Current Medicinal Chemistry 2001, 8, 829-838 829...

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